Purpose of review
Anemia is prevalent in patients with infections and other inflammatory conditions. Induction of the
iron regulatory hormone
hepcidin has been implicated in the pathogenesis of
anemia of
inflammation. This review outlines recent discoveries in understanding how
hepcidin and its receptor
ferroportin are regulated, how they contribute to
anemia of
inflammation, and how this knowledge may help guide new diagnostic and therapeutic strategies for this disease.
Recent findings
IL-6 is a primary driver for
hepcidin induction in many models of
anemia of
inflammation, but the SMAD1/5/8 pathway also contributes, likely via Activin B and SMAD-STAT3 interactions at the
hepcidin promoter.
Hepcidin has an important functional role in many, but not all forms of
anemia of
inflammation, although
hepcidin-independent mechanisms also contribute. In certain populations,
hepcidin assays may help target therapy with
iron or erythropoiesis-stimulating agents to patients who may benefit most. New therapies targeting the
hepcidin–
ferroportin axis have shown efficacy in preclinical and early clinical studies.
Summary
Recent studies confirm an important role for the
hepcidin–
ferroportin axis in the development of
anemia of
inflammation, but also highlight the diverse and complex pathogenesis of this disorder depending on the underlying disease.
Hepcidin-based diagnostic and therapeutic strategies offer promise to improve
anemia treatment, but more work is needed in this area.
